Scientists Greatly Simplify Model of how cancer Starts

The Two Researchers, Mike Khan and Stella Pelengaris

Originally published 13 May 2002

It is a double good news day for University of Warwick’s New BioMedical Research Institute. On the same day (Tuesday 14th May 2002) that Lord Wolfson comes to open the new Institutes’ Wolfson wing the new institutes’ researchers have announced that they have greatly simpified the model of how cancer starts.

Researchers in the University of Warwick’s Molecular Medicine Research Centre have undermined the old complex model of how many cancers start and identified a single protein known as c-Myc as a “mission-critical target for effective cancer therapies.”

Current cancer models suggest that a network of several cell mutations is needed to begin a cancer such a complex origin makes it difficult to find simple causes or easy targets that can be tackled. Treatment of developed cancers often have thus to be aggressive therapies to destroy the cancerwith high risks of damage to healthy tissue.

But new work by Dr. Stella Pelengaris, and Dr Mike Khan at the University of Warwick’s Molecular Medicine Research Centre has undermined the old complex model of how a cancer start and identified a single protein known as c-Myc as a “mission-critical target for effective cancer therapies.”

c-Myc is a protein which when switched on grows more cells when the body needs them. Sometimes it fails to switch off or switches itself on when it is not wanted. Normally our bodies have a fail safe mechanism which causes cells to commit suicide if c-Myc malfunctions in this way. This switching on of c-Myc and the failure of the cell suicide mechanism are two of the mutations required to start a cancer. However many researchers currently believe that many more mutations are also required if a cancer is to develop, for instance a mutation for developing a new blood supply required to nourish the growing cancer and mutation to allow cancerous cells to escape, travel the body and spread the cancer etc.

The researchers were not convinced by the need for a complex set of mutations and decided see what would happen if they introduced to pancreatic cells just the two mutations that would create the uncontrolled c-Myc. Their experiments showed that they were correct and that within days a cancer was established just by switching on the c-Myc to build more unwanted cells and inhibiting the cells suicide fail safe mechanism.

Dr Pelengaris said "People think cancer is very complicated, that you need half a dozen genetic lesions in order to get invasion. Our research provides a much more optimistic model. We've simplified it. We're saying that cancer isn't as complicated as people first thought." c-Myc may be one of several "mission-critical targets for effective cancer therapies.”

This research finds that cancer can have simple non complex causes that give us more optimism in developing forms of treatment - but if they are not detected early enough cancers can still develop a complexity that is difficult to defeat.